ABSTRACT We present a case of anaphylactic shock induced by exercise following celery ingestion. The possible mechanism of food-dependent exercise-induced anaphylaxis (FDEIA) and the laboratory tests for its diagnosis are discussed. We evaluated spontaneous, celery-allergen-induced, and anti-FcepsilonRI-antibody-induced histamine release from basophils obtained from the patient, 2 celery-allergic controls, and 3 healthy controls. Buffers of increasing osmolarity were used to mimic conditions of vigorous physical exercise. Only the patient's basophils showed an increase in spontaneous, anti-FcepsilonRI antibody-induced and allergen-induced histamine release under physiological conditions and with slightly increased medium osmolarity. To our knowledge, this is the first report on the possible role of increased histamine releasability in the pathogenic mechanism of FDEIA. We suggest that FDEIA results from increased histamine releasability triggered by physical effort after exposure to a sensitizing food allergen.

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Anaphylaxis is the systemic and most severe presentation of type I allergy. A number of conditions were identified that modulate the onset of anaphylaxis such as co- or augmentation factors, which significantly lower the allergen dose necessary for triggering anaphylaxis. Next to physical exercise or alcohol consumption, co-administration of nonsteroidal anti-inflammatory drugs (NSAID) or concomitant infectious diseases are well-documented cofactors of anaphylaxis. Registries for anaphylaxis document a role for cofactors in about 30% of anaphylactic reactions. Some disease entities such as 'wheat-dependent exercise-induced anaphylaxis' (WDEIA) are explicitly characterized by elicitation of anaphylaxis only in the presence of at least one such cofactor. Using WDEIA as a model disease, studies demonstrated that exercise increases skin prick test reactivity to and bioavailability of the allergen. Additional data indicate that alcohol consumption and NSAID administration display similar effects. Modulation of the cellular activation threshold is another mechanism underlying cofactor-induced anaphylaxis, most likely also functional when infectious diseases orchestrate elicitation of anaphylaxis. Cofactors are increasingly accepted to play a fundamental role in eliciting anaphylaxis. Consequently, to improve patient management modalities, a better understanding of the underlying mechanisms is warranted. This review aims to update clinicians and clinical scientists on recent developments.

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This article offers a review of the potential influences of personal lifestyle on respiratory health in children, looking at both healthy individuals and those with respiratory disorders. As with many aspects of health, regular physical activity, an appropriate diet, and avoidance of obesity and cigarette smoke all contribute to optimal development of the healthy child. An active lifestyle is associated with greater static and dynamic lung volumes, greater efficiency of the ventilatory process, and an optimization of breathing patterns. The risk of upper respiratory infections is also reduced in those maintaining a moderate level of physical activity. Maternal smoking during pregnancy, as well as active and passive smoking, all have an adverse influence on lung function in the child, the largest effects being on dynamic lung volumes. The risk of developing asthma seems reduced in children who maintain a normal body mass and are physically active. A program of graded physical activity is of therapeutic value in a number of established respiratory conditions, including asthma, cystic fibrosis, and ventilatory impairment from neuromuscular disorders. Exercise carries a slight risk of fatalities from asthma and anaphylactic reactions. In designing an optimal physical activity program, it is also important to guard against the hazards of deep oronasal breathing, including the precipitation of bronchospasm by the inhalation of cold, dry air and pollens; an increased exposure to atmospheric pollutants (reducing and oxidant smog, fine and ultra-fine particulates, and carbon monoxide); and possible long-term dangers from chlorine derivatives in the atmosphere of indoor swimming pools.

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We present two cases of food and exercise-induced anaphylaxis (FEIA) in patients with a diagnosis of oral allergy syndrome (OAS) to the implicated foods. Patient A had FEIA attributed to fresh coriander and tomato and Patient B to fresh celery. These food allergens have been implicated in OAS and have structural antigenic similarity to that of birch and/or grass. Both patients' allergies were confirmed by fresh skin prick tests. In both cases, strenuous exercise was antecedent to the systemic anaphylaxis reaction and subsequent ingestion without exercise produced only local symptoms of perioral pruritus. We review the current proposed mechanisms for food and exercise induced anaphylaxis to oral allergens and propose a novel and more biologically plausible mechanism. We hypothesize that the inhibitory effects of exercise on gastric acid secretion decreases the digestion of oral allergens and preserves structural integrity, thereby allowing continued systemic absorption of the allergen whether it be profilins, lipid transfer proteins, or other antigenic determinants.

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Spontaneous Histamine Release Antibody-Induced Histamine Release Allergen-Induced Histamine ReleaseOsmolarity (mOsm) 280 340 450 280 340 450 280 340 450Patient, % 9.57 15.07 12.16 72.69 84.90 51.32 7.41 16.59 1.46Mean Healthycontrols, % 2.23 3.67 1.22 15.22 15.88 18.56 0.02 0.06 0.7Mean: Celery-allergic controls, % 2.75 2.7 8.25 87.95 86.55 87.2 16.35 13.25 74.4angioedema, urticaria, and generalized pruritus. The event took place while she was playing ball 1 hour after ingesting fresh celery. She recovered after routine treatment with adrenaline, corticosteroids, and phenazoline. The patient had previously been diagnosed with asthma and seasonal allergic rhinitis, and was on regular inhaled treatment (long-acting ß2-agonists, corticosteroids, chromones) and oral treatment (montelukast and cetirizine). Skin prick tests were positive to mugwort pollens and house dust mites, but she never underwent specifi c immunotherapy. One year previously, she attended the emergency room due to angioedema of the upper airway with no systemic symptoms. The event took place during a wedding party, but the trigger was not identifi ed. The patient’s allergologic status was evaluated a few months after the anaphylactic shock and a skin prick test for celery was positive. In contrast, the specifi c immunoglobulin (Ig) E test (both Allergopharma, Reinbek, Germany) was negative. An exercise test was performed, but it induced neither symptoms of anaphylaxis nor signifi cant spirometric fi ndings. Because of the life-threatening anaphylactic reaction, an exercise challenge after celery ingestion was not performed. We compared histamine releasability from basophils obtained from the patient with that of 3 healthy controls and that of 2 celery-allergic patients who tolerated exercise. It is known that increased medium osmolarity increases both IgE-dependent and IgE-independent histamine releasability from basophils [3,4]. It is also known that increased osmolarity due to intensive physical effort results in amplifi ed release of mediators of allergic reactions [5]. Thus, the histamine release tests were performed using a range of buffers with increasing osmolarity–280 mOsm, 340 mOsm, and 450 mOsm–to mimic conditions of vigorous physical exercise. Increased osmolarity was achieved by the addition of mannitol. The venous blood specimens were collected on EDTA and mixed with dextran solution in the proportion 4:1 (Bühlmann Laboratories AG, Schönenbuch, Switzerland). After 90 minutes of sedimentation at room temperature, the upper phase was transferred into a second tube and centrifuged for 15 minutes at 130g at room temperature. After the supernatant was discarded, cells were suspended at a concentration of 1 ? 107/mL of the stimulation buffer (Bühlmann Laboratories AG). Histamine release was induced by celery allergen at a fi nal concentration of 20 ng/mL, and by anti-FcεRI monoclonal antibody (both from Bühlmann Laboratories AG). In order to determine spontaneous histamine release (SHR), blood cells were incubated only in stimulation buffer (Bühlmann Laboratories AG). After 40 minutes of incubation at 37?C, the samples were centrifuged at 4?C at 1000g for 3 minutes and the supernatants were tested for histamine concentration. Total histamine content was determined in separate tubes after incubation in Triton X100. The histamine concentration in the samples was determined by Histamine-ELISA (IBL, Hamburg, Germany). All measurements were made in duplicate and the values averaged. The results in the cell samples stimulated with celery allergen and anti-FcεRI monoclonal antibody are expressed in percentages after subtraction of the SHR values. The positivity cutoff was set at 5%.In the healthy controls, SHR at physiological osmolarity (280 mOsm) was very low (mean, 2.2%). The increase in medium osmolarity to 340 mOsm and 450 mOsm did not markedly change the SHR values. In the celery-allergic controls, SHR remained at the same low level at physiological osmolarity and at 340 mOsm, and increased to 8.2% at the highest medium osmolarity. However, the patient’s basophils exhibited a much higher SHR at physiological osmolarity (9.6%). Increasing medium osmolarity produced an increase in SHR to 15% at 340 mOsm. This remained high at 450 mOsm. Similar differences were observed when the basophils were stimulated by anti-FcεRI monoclonal antibody. The patient’s basophils exhibited very high histamine release values at physiological osmolarity, which increased slightly with osmolarity (340 mOsm). However, further increases in buffer osmolarity to 450 mOsm led to a decrease in histamine release. In the celery-allergic controls, anti-FcεRI-induced histamine release was very high and did not change when osmolarity increased. In the healthy controls, anti-FcεRI-induced histamine release remained low in 1 person at all medium osmolarities. In 2 others it was positive, but was not clearly infl uenced by increasing osmolarity to 340 mOsm. Further increases in medium osmolarity to 450 mOsm resulted in